JOURNAL OF SHANDONG UNIVERSITY (OTOLARYNGOLOGY AND OPHTHALMOLOGY) ›› 2015, Vol. 29 ›› Issue (6): 56-59.doi: 10.6040/j.issn.1673-3770.0.2015.215

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The experiment of SIRT1 on against oxidative stress to retinal pigmented epithelium cells

LI Langen1, WEI Wei1, ZHANG Yufeng1, Geriletu1, YANG Jia2, ZHANG Yanmei3   

  1. 1. Departments of Ophthalmology, Inner Mongolia People's Hospital, Hohhot 010017, Inner Mongolia, China;
    2. Departments of Neurology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010000, Inner Mongolia, China;
    3. Departments of Neurology, Inner Mongolia People's Hospital, Hohhot 010017, Inner Mongolia, China
  • Received:2015-06-02 Online:2015-12-16 Published:2015-12-16

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Abstract: Objective To observe the protection role of the sirtuin 1 (SIRT1) towards the retinal pigmented epithelium(RPE) cells following exposure to oxidative stress. Methods The rates of proliferation and apoptosis, levels of intracellular reactive oxygen species(ROS) and cell senescence of RPEs, induced by oxidants (H2O2), were evaluated. Results The results revealed a down-regulation of SIRT1 expression during oxidative stress. Furthermore, SIRT1 activator resveratrol (RSV) and inhibitors nicotinamide (NA) were respectively treated on RPE cells following exposure by H2O2 intervention; the expression of SIRT1 gene were detected by RT-PCR technology after RNA interfering on SIRT1. The experiments indicated that cell proliferation, apoptosis and ROS levels were significantly different compared with the control group after intervention by H2O2, and cell senescence were significantly increased; NA was significantly increased the toxicity of H2O2, however RSV had the opposite anti-cytotoxicity of H2O2; RT-PCR analysis showed that SIRT1 levels were significantly reduced. Conclusion These results therefore suggested that down-regulation of SirT1 expression during oxidative stress, further investigation indicated that SIRT1 protected RPEs from oxidative stressinduced damage. Appropriate increase of the activity of SIRT1 may be a therapeutic strategy to delay AMD.

Key words: H2O2, Cell growth, Silent information regulator of transcription 1, Retinal pigmented epithelium cells, Reactive oxygen species, siRNA, Oxidative stress

CLC Number: 

  • R774
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